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1 2 Otoacoustic Emissions Textbook • Overview of otoacoustic emissions • Anatomy and physiology • Classification of OAEs • Instrumentation and calibration • Clinical measurement of OAEs: procedures • OAE analysis • OAE applications in children • OAE applications in adults • Efferent auditory system and OAEs • New directions in research and clinical application • • 3 4 5 6 OAEs in AUDIOLOGY TODAY: Main Points OAEs are important in the diagnostic audiologic assessment of children and adults. OAE findings and the audiogram do not always agree … that’s good … OAEs provide unique information on auditory status. Abnormal OAEs can be recorded with a normal audiogram … and can detect cochlear dysfunction. OAEs should be a part of the basic audiologic test battery. Giuseppe Tartini (April 8, 1692 - February 26, 1770) 7 8 9 OAE: Classic Quote from Yesteryear by Thomas Gold “I had discussed at length in 1948 with von Bekesy at Harvard that the observations he made on the dead cochlea were unrepresentative. But he wouldn’t have that!” “It is shown that the assumption of a ‘passive’ cochlea, where the elements are brought into mechanical oscillation solely by means of the incident sound, is not tenable.” 10 “ … the nerve ending abstracts much energy from a mechanical resonator.” William Rhode demonstrates cochlear nonlinearity in the squirrel monkey in 1971. 11 12 Discovery of OAEs by David Kemp (Kemp DT. Stimulated acoustic emissions from within the human auditory system. JASA 64: 1978.) “A new auditory phenomenon has been identified in the acoustic impulse of the human ear… This component of the response appears to have its origin in some nonlinear mechanism probably located in the cochlea, responding mechanically to auditory stimulation, and dependent upon the normal functioning of the cochlear transduction process… It is tempting to suggest that one of the functions of the outer hair cell population is the generation of this mechanical energy.” 13 14 15 16 17 Historical Overview of OAEs: Major Events Since Discovery (1) 1980s Early studies of newborn hearing screening in UK and Denmark Introduction of ILO 88 “auditory neuropathy” 1990s Research on DPOAEs in animals and humans NIH Consensus Conference recommends UNHS in 1993, including use of OAEs New DPOAE systems by major manufacturers in 1994 First CPT codes in 1995 OAEs in identification of ANSD Automated OAE devices Evidence on clinical applications grows Historical Overview of OAEs: Major Events Since Discovery (2) 2000 to present Two textbooks on OAEs OAEs recommended by JCIH for screening New applications of OAEs including: Tinnitus Ototoxicity monitoring Noise/music cochlear dysfunction Preschool and school age screening Combination technologies ABR and OAEs Tympanometry and OAEs New CPT codes for OAEs 18 19 20 OAEs: Differences between inner and outer hair cells (1) Inner Hair Cells Outer Hair Cells Single row 3 or 4 rows N = 3500 N = 12,000 to 20,000 On spiral lamina On basilar lamina Wine bottle shape Cylinder (test tube) shape) No contact bet/ stereocilia Tallest stereocilia contact tectorial and tectorial membrane membrane 95% of afferents innervate IHC 5% of afferents innervate OHCs 21 OAEs: Differences between inner and outer hair cells (2) Inner Hair Cells Not motile Outer Hair Cells Motile Encompassed by support cells Supported only on top & bottom Central nucleus Nucleus at base of cell Single layer of endoplasmic Extensive subsurface reticulum cisternae Mitochondria scattered Mitochondria along throughout cell perimeter Efferents from lateral Efferents from medial superior olive superior olive 22 23 24 Site of Generation Cochlea: observed delay in OAEs; recordings from BM & auditory nerve. Outer Hair Cells: concomitant ablation of OAEs and OHC (e.g., Davis et. al., 2002); loss of OAEs due to other insults associated with OHC damage (salicylate, noise, etc.). But where in the OHC? 25 26 Site of Generation Cochlea: observed delay in OAEs; recordings from BM & auditory nerve. Outer Hair Cells: concomitant ablation of OAEs and OHC (e.g., Davis et. al., 2002); loss of OAEs due to other insults associated with OHC damage (salicylate, noise, etc.). But where in the OHC? 27 28 29 30 31 32 33 Why does it matter? No amplifier: Recordable DPOAEs at high input levels. Good candidate for acoustic amplification. No transducer: DPOAEs not recordable. Good candidate for electrical input. Auditory Anatomy Involved in the Generation of OAEs Outer hair cell motility Prestin motor protein Stereocilia Motion Stiffness Tectorial membrane Basilar membrane mechanics Dynamic interaction with outer hair cells Stria vascularis Middle ear (inward and outward propagation) Medial efferent pathways External ear canal Stimulus presentation OAE detection 34 35 36 CLINICAL APPLICATION OF OTOACOUSTIC EMISSIONS (OAE): General advantages 37 38 39 40 41 42 Highly sensitive to cochlear (outer hair cell function) Site specific (to outer hair cells) Do not require behavioral cooperation or response Ear specific Highly frequency specific Do not require sound-treated environment Can be quick (< 30 seconds) Portable (handheld devices) Relatively inexpensive CLINICAL APPLICATION OF OTOACOUSTIC EMISSIONS (OAE): Possible disadvantages Susceptible to effects of noise Affected greatly by middle ear status Provide cochlear information only about outer hair cells May be abnormal or not detected with normal audiogram Are not detectable with hearing loss > 40 dB HL Cannot be used to estimate degree of hearing loss Not a measure of neural or CNS auditory function Not a test of hearing Outer Hair Cells, Otoacoustic Emissions, and Auditory Function OHCs and OAEs are highly dependent on blood flow to the cochlea, due to demands of metabolism OAEs are pre-neural and, therefore, not affected by retrocochlear auditory dysfunction OHC motility contributes to: enhanced auditory sensitivity sharper tuning curves (increased frequency selectivity or cochlear tuning) normal growth of loudness OAEs after Sound Induced Damage And in humans… still from Avan & Bonfils (2004) Recreational Exposure 43 44 45 46 47 48 49 50 Six Reasons Why OAEs Will Never Replace the Audiogram nor Accurately Estimate Hearing Loss (1-3) OAEs measurement is dependent on inward and outward propagation of energy through the middle ear (e.g., abnormal OAEs with normal hearing sensitivity) OAEs are more sensitive to cochlear dysfunction than the audiogram (e.g., abnormal OAEs with normal hearing sensitivity) OAEs are electrophysiologic measures while the audiogram is behavioral (e.g., normal OAEs with abnormal audiogram) 51 Six Reasons Why OAEs Will Never Replace the Audiogram nor Accurately Estimate Hearing Loss (4-6) OAEs are produced by OHCs, whereas the audiogram is dependent on IHCs (e.g., normal OAEs with abnormal audiogram) OAEs are pre-neural, whereas the audiogram is dependent on retrocochlear pathways (e.g., normal OAEs with abnormal hearing sensitivity) OAEs reflect OHC integrity, whereas the audiogram measure hearing (e.g., normal OAEs with abnormal audiogram) 52 Otoacoustic Emissions in Audiology Today: Limitations in use of OAEs by clinical audiologists 53 54 55 56 57 Regular Spacing of Spontaneous OAEs Coherent Reflection Filtering 58 59 60 Classification Types of OAEs: Conventional Classification Type Stimulus Spontaneous none Prevalence < 70% Evoked transient click or tone burst > 99% distortion product two pure tones > 99% stimulus frequency continuous tone ?? % 61 Transient Otoacoustic Emissions (TEOAE) 62 63 64 65 Distortion Product Otoacoustic Emissions (DPOAEs) 66 67 68 69 70 71 72 73 74 Mixed DPOAEs 75 76 77 78 79 80 Improving Predictions Using I/O Functions Plot DPOAE pressure (in Pascals not dB SPL). Fit linear function to first few points reliably above the noise floor. Threshold is the stimulus level that yields 0 Pa DPOAE amplitude per the fitted line. (Boege & Janssen, 2002) Two slope method (Neely et al., 2009) leads to further improvement. 81 82 83 84 85 OAEs: Abnormal OHCs and loudness recruitment “The phenomenon of loudness recruitment appears to be the psychoacoustic expression of the loss of a large component of outer hair cells and the concurrent preservation of a large component of inner hair cells and type I cochlear neurons.” Schuknecht HF. Pathology of the Ear (2nd ed). 1993, p. 91 86 87 88 89 90 91 Steps in Analysis of DPOAE Findings Perform analysis at all test frequencies Verify adequately low noise floor (< 90% normal limits) Verify replicability of DPOAE amplitude (+/- 2 dB) from at least two runs Is DP - NF difference > 6 dB? Yes? DPOAEs are present No? There is no evidence of DPOAEs Is DP amplitude within normal limits? Yes? DPOAEs are normal No? DPAOEs are abnormal (but present) EAR CANAL FACTORS INFLUENCING OAE MEASUREMENT Non-pathologic probe tip placement, size, or condition probe insertion depth standing waves cerumen or debris vernix casseous (healthy newborn infants) Pathologic stenosis external otitis CLINICAL APPLICATION OF OTOACOUSTIC EMISSIONS (OAE): Trouble-shooting Minimizing the effects of noise on OAE recordings eliminate extraneous noise sources in test room close door to test room insert probe deeply secure probe cord instruct patient to remain quiet and still (if feasible) position test ear away from equipment modify protocol (to frequencies > 2000 Hz) VENTILATION TUBES and OAEs Daya et al. (1966). Otoacoustic emissions: Assessment of hearing after tympanostomy tube insertion. Clin Otolaryngol 21: 492-494. Owens, McCoy, Lonsbury-Martin, Martin. (1993). Otoacoustic emissions in children with normal ears, middle ear dysfunction, and ventilating tubes. Amer J Otol 14: 34-40. Tilanus. Stenis, Snik.(1995). Otoacoustic emission measurements in evaluation of the effect 92 of ventilation tube insertion in children. Annals of ORL 104: 297-300. Richardson, Elliott, Hill. (1996). The feasibility of recording transiently evoked otoacoustic emissions immediately following grommet insertion. Clin Otolaryngol 21: 445-448. Cullington, Kumar, Flood. (1998). Feasibility of otoacoustic emissions as a hearing screen following grommet insertion. Brit J Audio 32: 57-62. AUDIOGRAM & DPOAEs: Pre-ventilation tubes (5 y.o. girl) 93 94 95 96 97 AUDIOGRAM & DPOAEs: Ventilation tubes (4 mos. later before APD eval.) Non-factors in OAE Interpretation Non-Factors diurnal effects (time of day) genetics body temperature body position anesthetic agents (w/ normal middle ear status) state of arousal (attention to stimulus) 98 99 100 101 Six Reasons Why OAEs Will Never Replace the Audiogram nor Accurately Estimate Hearing Loss (1-3) OAEs measurement is dependent on inward and outward propagation of energy through the middle ear (e.g., abnormal OAEs with normal hearing sensitivity) OAEs are more sensitive to cochlear dysfunction than the audiogram (e.g., abnormal OAEs with normal hearing sensitivity) OAEs are electrophysiologic measures while the audiogram is behavioral (e.g., normal OAEs with abnormal audiogram) 102 Six Reasons Why OAEs Will Never Replace the Audiogram nor Accurately Estimate Hearing Loss (4-6) OAEs are produced by OHCs, whereas the audiogram is dependent on IHCs (e.g., normal OAEs with abnormal audiogram) OAEs are pre-neural, whereas the audiogram is dependent on retrocochlear pathways (e.g., normal OAEs with abnormal hearing sensitivity) OAEs reflect OHC integrity, whereas the audiogram measure hearing (e.g., normal OAEs with abnormal audiogram) 103 104 105 106 107 Functional Role of Auditory Efferents Protection from noise. Disrupted function in neuropathy. Role in learning and learning disability. Signal detection and localization in noise. 108 109 110 111 112 113 114 115 116 117 118 CAS leads to reduction in SOAE magnitude and increase in SOAE frequency 119 120 121 122 123 124 125 126 127 The direction of change in SOAE level and frequency reflects changes in BM vibration magnitude and phase. Slow effects are minuscule if any. Changes in SOAE frequency shows an “intermediate effect.” Absence of slow effects detracts from role in protection from noise trauma. Tuning of MOC Efferents 128 129 130 131 132 133 134 135 136 Contralateral tones near 750 Hz appear to be most effective in inhibiting SOAEs of all frequencies. Cat MOC fibers have a second lobe of sensitivity at a lower frequency. These data would suggest that this secondary lobe is dominant in humans (and the primary tuning peak is absent). Could be a difference due to anesthesia. Then we could be witnessing the effect of the entire cortico-fugal system in the human, versus the olivocochlear system in cats. Distortion Product OAEs 137 138 139 140 General Methods • 8 normal-hearing young adults. • Best estimate of middle ear muscle reflex > 90 dB SPL. • DPOAE recorded using stimulus tones swept in frequency between 1 and 4 kHz. • Broad band noise (0.1 - 10 kHz) presented in contralateral ear at 60, 70, and 80 dB SPL. • +CAS conditions bracketed by two -CAS conditions. 141 142 Greater reduction in CF component could explain DPOAE enhancement in valleys. 143 144 The magnitude of the CF component is reduced more than the magnitude of the overlap component on efferent stimulation (also observed by Abdala et al., 2009). Efferent stimulation also causes fine structure patterns to shift toward higher frequencies. (Mauermann & Kollmeier, 2004; Sun, 2005, 2008; Purcell et al., 2008, Abdala, 2009) 145 146 147 Change in slope of CF component phase. Change in slope of CF component phase. 148 149 CF component phase changes more than overlap component phase on efferent activation. 150 151 152 153 154 155 Clinical Considerations Stuck at one frequency Following a peak Tracking frequency shift Practically speaking... 156 Efferent modulation of OAEs can be complex with changes in both magnitude and phase. Both clinicians and scientists appear to be interested in the phenomenon and its reliable measurement. 157 Questions?